Topography of focal proximal tubular necrosis after ischemia with reflow in the rat kidney.

PF Shanley, MD Rosen, M Brezis, P Silva… - The American journal …, 1986 - ncbi.nlm.nih.gov
PF Shanley, MD Rosen, M Brezis, P Silva, FH Epstein, S Rosen
The American journal of pathology, 1986ncbi.nlm.nih.gov
The topography of renal injury after ischemia-reflow was studied in intact rats by clamping
the right renal artery for variable periods of time and examining the histologic appearance of
the kidney in large 1-mu plastic sections. As reported by others, the straight portion of the
proximal tubule (S3) was especially susceptible to ischemia-reflow injury. The pattern of
focal necrosis produced in S3 by short (15-30-minute) and longer (45-60-minute) periods of
arterial occlusion appeared related to gradients to oxygenation during reflow, in that more …
Abstract
The topography of renal injury after ischemia-reflow was studied in intact rats by clamping the right renal artery for variable periods of time and examining the histologic appearance of the kidney in large 1-mu plastic sections. As reported by others, the straight portion of the proximal tubule (S3) was especially susceptible to ischemia-reflow injury. The pattern of focal necrosis produced in S3 by short (15-30-minute) and longer (45-60-minute) periods of arterial occlusion appeared related to gradients to oxygenation during reflow, in that more extensive injury was seen in areas remote from blood vessels, while perivascular tubules were protected. A similar pattern was seen in S1 and S2 after a longer period (45-60-minutes) of ischemia, which produced extensive but incomplete necrosis in these convoluted segments, with protected tubules lying within zones surrounding arcuate and interlobular arteries. The immediate postglomerular portion of S1, a tubular segment normally well supplied with oxygen, was an exception to this rule. Selective necrosis limited to this portion of the nephron appeared after only 15-30 minutes of ischemia, recalling the special sensitivity of S1 cells to inhibition of mitochondrial respiration. These results suggest that in different segments of the proximal tubule, injury after ischemia-reflow is determined not only by changes that occur during complete ischemia but also by the adequacy of oxygenation during the reflow period.
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